PubMed Health⌕ Search

Biomedical subjects

Jean Guibourdenche

Publications and source records attributed to Jean Guibourdenche.

17 recordsLinked to original sources
PubMed2006

Biochemical investigations of bowel inflammation in gastroschisis.

Neonates with gastroschisis have perivisceritis resulting from contact between the bowel and amniotic fluid. Here, we characterized the mediators involved in this inflammatory process in humans and ewes, to find a reliable marker of this process. We have diagnosed 41 cases of gastroschisis since 1995. Amniotic fluid sampled for karyotyping between 15 and 32 wk of gestation was also used to assay cytokines and inflammatory proteins. The findings were compared with those in 93 age-matched controls. Amniotic fluid cells were analyzed by means of cytology. Histologic examination of the bowel was performed when neonatal appendectomy was performed. The findings were compared with those obtained in a ewe model of gastroschisis. In gastroschisis, amniotic total protein, IL-6, IL-8, and ferritin levels were significantly higher than in controls. Gastroschisis was associated with significantly higher cell counts (mainly mononuclear cells) in amniotic fluid. At birth, macrophages were abundant in the fibrous peel covering the bowel. Similar results were obtained in the ewe model. Gastroschisis may be associated with a subchronic inflammatory process of variable intensity. This inflammation is restricted to the bowel wall and involves inflammatory cells such as macrophages, which may secrete ferritin, neopterin, and calprotectin.

Amniotic Fluid↗
PubMed2006

Congenital hyperthyroidism: the fetus as a patient.

Congenital hyperthyroidism is less frequent than congenital hypothyroidism but its impact on growth and development can be as dramatic. The immune form of hyperthyroidism that is transmitted from a mother with Graves' disease to her foetus and then neonate is transient, but cases of persistent congenital hyperthyroidism had also been described, that can now be explained by molecular abnormalities of the thyrotropin receptor. The abundance of published data on the neonatal effects of maternal Graves' disease contrasts with the paucity of information on fetal effects. Recent studies showed that it is of utmost to scrutinize fetal thyroid by expert ultrasonographist and to have a team work with obstetricians and pediatric endocrinologists in pregnant women with Graves' disease. This allowed to accurately determine the fetal thyroid status and to adapt the treatment in the mothers successfully. Fetal hyperthyroidism does exist and needs an appropriate aggressive treatment. Clearly the fetus has become our patient!

Female↗
PubMed2005

Management of Graves' disease during pregnancy: the key role of fetal thyroid gland monitoring.

BACKGROUND: Fetuses from mothers with Graves' disease may experience hypothyroidism or hyperthyroidism due to transplacental transfer of antithyroid drugs (ATD) or anti-TSH receptor antibodies, respectively. Little is known about the fetal consequences. Early diagnosis is essential to successful management. We investigated a new approach to the fetal diagnosis of thyroid dysfunction and validated the usefulness of fetal thyroid ultrasonograms. METHODS: Seventy-two mothers with past or present Graves' disease and their fetuses were monitored monthly from 22 wk gestation. Fetal thyroid size and Doppler signals, and fetal bone maturation were determined on ultrasonograms, and thyroid function was evaluated at birth. Thyroid function and ATD dosage were monitored in the mothers. RESULTS: The 31 fetuses whose mothers were anti-TSH receptor antibody negative and took no ATDs during late pregnancy had normal test results. Of the 41 other fetuses, 30 had normal test results at 32 wk, 29 were euthyroid at birth, and one had moderate hypothyroidism on cord blood tests. In the remaining 11 fetuses, goiter was visualized by ultrasonography at 32 wk, and fetal thyroid dysfunction was diagnosed and treated; there was one death, in a late referral, and 10 good outcomes with normal or slightly altered thyroid function at birth. The sensitivity and specificity of fetal thyroid ultrasound at 32 wk for the diagnosis of clinically relevant fetal thyroid dysfunction were 92 and 100%, respectively. CONCLUSION: In pregnant women with past or current Graves' disease, ultrasonography of the fetal thyroid gland by an experienced ultrasonographer is an excellent diagnostic tool. This tool in conjunction with close teamwork among internists, endocrinologists, obstetricians, echographists, and pediatricians can ensure normal fetal thyroid function.

Adult↗
PubMed2005

Stimulation of human trophoblast invasion by placental growth hormone.

A critical step in establishment of human pregnancy is the invasion of the uterus wall by the extravillous cytotrophoblast (EVCT), a process regulated by multiple autocrine and paracrine factors. Hormones belonging to the GH/prolactin family are expressed at the maternofetal interface. Because they are involved in cell motility in various models, we examined the possible regulatory role of human placental GH (hPGH) in EVCT invasiveness. By using an in vitro invasion model, we found that EVCT isolated from first-trimester chorionic villi and cultured on Matrigel secreted hPGH and expressed human GH receptor (hGHR). These data were confirmed by in situ immunohistochemistry. EVCT expressed the full-length and truncated forms of hGHR, and the Janus kinase-2/signal transducer and activator of transcription factor-5 signaling pathway was activated in EVCT by hPGH treatment. Strong hPGH and hGHR expression was observed when EVCT invaded Matrigel and moved through the pores of the filter on which they were cultured. hPGH stimulated EVCT invasiveness, and this effect was inhibited by a Janus kinase-2 inhibitor. Interestingly, hPGH was more efficient than pituitary GH in stimulating EVCT invasiveness. These results offer the first evidence for a placental role of hPGH and suggest an autocrine/paracrine role of hPGH in the regulation of trophoblast invasion.

Cells, Cultured↗
PubMed2005

Prenatal diagnosis of megacystis-microcolon-intestinal hypoperistalsis syndrome: contribution of amniotic fluid digestive enzyme assay and fetal urinalysis.

OBJECTIVES: Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) is a usually lethal disease during the first year of life. There is no specific ultrasound prenatal diagnosis and no identified genetic locus. The value of amniotic fluid digestive enzyme assay and fetal urine biochemistry in the prediction of MMIHS was analysed. METHODS: Retrospective study of 14 MMIHS cases. Amniotic fluid digestive enzymes and fetal urine biochemistry were compared in MMIHS and megabladder (63 and 264 cases respectively). RESULTS: Abnormal amniotic fluid digestive enzyme profile (vomiting of bile or digestive secretion leakage) was observed in 8/10 MMIHS cases. These profiles were observed in 7/63 controls; 80% sensitivity (95%CI = 55%-100%); 89% specificity (95%CI = 81%-96%). Fetal urinalysis was normal in 12/12 MMIHS cases except high calcium (>0.6 mmol/l). This profile was observed in 33/264 megabladder control cases; 100% sensitivity; 98.7% specificity (95%CI = 83.5%-91.5%). CONCLUSION: For the first time, we propose a prenatal diagnosis of MMIHS based on amniotic fluid digestive enzyme assay and on fetal urinalysis.

Adolescent↗
PubMed2005

Gastroschisis.

Explore the source record for details and available documents.

Cardiotocography↗
PubMed2005

Thyroid function during pregnancy in women with past Graves' disease.

Graves' disease and thyroid dysfunction during pregnancy can lead to maternal and fetal complications. No information is available on thyroid function in women with a past history of Graves' disease. We compared free T3, free T4 and TSH in a group of pregnant women with a history of resolved Graves' disease requiring no current treatment (n= 34) and in a group of pregnant controls (n= 102). We found no significant differences in the levels of these hormones between the two groups. Women with a past history of Graves' disease and no current treatment display a normal thyroid function and adaptation during pregnancy.

Adult↗
PubMed2005

Fetal anal incontinence evaluated by amniotic fluid digestive enzyme assay in myelomeningocele spina bifida.

The goals of this study were to determine whether anal sphincter dysfunction in spina bifida develops during fetal life or after birth and whether it reflects the severity of spina bifida and therefore can be used as a criterion to select the cases that could benefit from in uterosurgery. Total protein and digestive enzyme activities [gamma-glutamyl transpeptidase (GGTP), aminopeptidase M (AMP), and alkaline phosphatase isoenzymes including the intestinal form (iALP)] were assayed retrospectively in amniotic fluid from 80 myelomeningocele spina bifida cases without unrelated associated malformation (gestational age 14-33 wk). A normal enzyme activity profile was observed in 46 of the 80 cases. Two abnormal profiles were observed: 1) bilious vomiting, characterized by abnormally high GGTP and AMP activities but normal iALP, and 2) digestive enzyme leakage, characterized by abnormally high activities of GGTP, AMP, and iALP, typical of anal incontinence. No relation was observed between these enzyme activity profiles and the different secondary signs of spina bifida or the level of the damage. In conclusion, anal sphincter dysfunction in spina bifida revealed by amniotic fluid digestive enzyme activities occurred before 24 wk in fetal life in 28.7% of cases. This criterion may be indicative of the severity of spina bifida and therefore perhaps could be used to select cases that are suited to in utero surgery. It could also be used to establish the potential benefit of this surgery in fecal incontinence.

Alkaline Phosphatase↗
PubMed2004

Amniotic fluid inflammatory proteins and digestive compounds profile in fetuses with gastroschisis undergoing amnioexchange.

OBJECTIVE: In gastroschisis, an inflammatory process related to the presence of digestive compounds may be involved in intestinal damage. We measured the amniotic fluid concentrations of total protein, ferritin and amylase, lipase, gamma-glutamyl transferase and bile acids before each amnioexchange performed in women whose infants had gastroschisis. We estimated the correlation among total proteins, ferritin and digestive compounds and postnatal outcome. DESIGN: All women whose infants had gastroschisis in our fetal medicine unit are offered repeated amnioexchange during the third trimester of pregnancy to improve the quality of the exteriorised bowel at birth. Amniotic fluid was sampled at the beginning of each amnioexchange and total proteins, ferritin and digestive compounds were assayed. SETTING: This study was conducted in the Department of Perinatology of the University Hospital Robert Debré in Paris. POPULATION: Thirty pregnant women with a gastroschisis affected fetus diagnosed antenatally. METHODS: The biological results were expressed as multiples of the median with respect to a control population. MAIN OUTCOME MEASURE: Gestational age at delivery and the outcome of the infants were recorded and correlated with amniotic fluid total proteins, ferritin and digestive compounds. RESULTS: There was a positive correlation (P < 0.01) between digestive compounds (except amylase at the final amnioexchange) and ferritin on the one hand, and all digestive compounds and total proteins concentration at the final amnioexchange on the other. In addition, among total proteins amylase and lipase, lipase concentrations were related with parameters of short term outcome (P < 0.05). CONCLUSION: Amniotic total proteins and ferritin are elevated in fetuses presenting with gastroschisis as a consequence of an inflammatory process. Inflammation may be induced by the presence of digestive compounds in the amniotic fluid. The concentrations of which may constitute a marker of short term outcome of the newborn infant.

Adolescent↗
PubMed2003

Involvement of connexin 43 in human trophoblast cell fusion and differentiation.

The syncytiotrophoblast is the principal component of the human placenta involved in feto-maternal exchanges and hormone secretion. The syncytiotrophoblast arises from the fusion of villous cytotrophoblasts. We recently showed that functional gap junctional intercellular communication (GJIC) is an important prerequisite for syncytiotrophoblast formation and that connexin 43 (Cx43) is present in cytotrophoblasts and in the syncytiotrophoblast. To determine whether Cx43 is directly involved in trophoblast fusion, we used an antisense strategy in primary cultures of human villous cytotrophoblasts that spontaneously differentiate into the syncytiotrophoblast by cell fusion. We assessed the morphological and functional differentiation of trophoblasts by desmoplakin immunostaining, by quantifying hCG (human chorionic gonadotropin) production and by measuring the expression of specific trophoblast genes (hCG and HERV-W). Furthermore, we used the gap-FRAP (fluorescence recovery after photobleaching) method to investigate functional GJIC. Cytotrophoblasts treated with Cx43 antisense aggregated and fused poorly. Furthermore, less HERV-W env mRNA, hCGbeta mRNA and hCG secretion were detected in Cx43 antisense-treated cytotrophoblasts than in cells treated with scrambled antisense. Treatment with Cx43 antisense dramatically reduced the percentage of coupled trophoblast cells. Taken together, these results suggest that Cx43 is directly involved in human trophoblast cell-cell communication, fusion and differentiation.

Cell Communication↗
PubMed2003

Requirement of gap junctional intercellular communication for human villous trophoblast differentiation.

During pregnancy, the villous trophoblast develops from the fusion of cytotrophoblastic cells (CT) into a syncytiotrophoblast (ST), supporting the main physiological functions of the human placenta. Connexin43 (Cx43) is demonstrated in situ and in vitro in the villous trophoblast between CT and between CT and ST. Moreover, the presence of a gap junctional intercellular communication (GJIC) during in vitro trophoblast differentiation was previously demonstrated. Because the exchange of molecules through gap junctions is considered to play a major role in the control of cell and tissue differentiation, we studied the effects of a gap junctional uncoupler, heptanol, on morphological and functional trophoblast differentiation and on GJIC measured by the fluorescence recovery after photobleaching method. We found that when the GJIC was interrupted, CT still aggregated but fused poorly. This morphological effect was associated with a significant decrease of trophoblastic-specific gene expression (beta human chorionic gonadotropin and human chorionic somatomammotropin). This blocking action was reversible as demonstrated by recovery of GJIC and trophoblast differentiation process after heptanol removal. Moreover, the inhibition of the trophoblast differentiation did not affect Cx43 transcript expression and Cx43 protein expression. These data suggest that the molecular exchanges through gap junctions preceding cellular fusion are essential for trophoblast differentiation generating the multifunctional syncytiotrophoblast.

Cell Communication↗
PubMed2003

Serum anti-Müllerian hormone is more strongly related to ovarian follicular status than serum inhibin B, estradiol, FSH and LH on day 3.

BACKGROUND: The study aim was to compare the relationship between serum anti-Müllerian hormone (AMH) levels and other markers of ovarian function with early antral follicle count on day 3. METHODS: A total of 75 infertile women was studied prospectively. On cycle day 3, serum levels of AMH, inhibin B, estradiol (E(2)), FSH and LH levels were measured, and the number of early antral follicles (2-10 mm in diameter) estimated at ultrasound scanning to compare the strengths of hormonal-follicular correlations. RESULTS: Median (range) serum levels of AMH, inhibin B, E(2), FSH and LH were 1.39 ng/ml (0.24-6.40), 90 (16-182) pg/ml, 31 (15-111) pg/ml, 7.0 (2.9-19.3) mIU/ml and 4.7 (1.2-11.7) mIU/ml respectively, and follicular count was 12 (1-35). Serum AMH levels were more strongly correlated (P < 0.001) with follicular count (r = 0.74, P < 0.0001) than were serum levels of inhibin B (r = 0.29, P < 0.001), E(2) (r = -0.08, P = NS), FSH (r = -0.29, P < 0.001) and LH (r = 0.05, P = NS). CONCLUSIONS: Serum AMH levels were more robustly correlated with the number of early antral follicles than inhibin B, E(2), FSH and LH on cycle day 3. This suggests that AMH may reflect ovarian follicular status better than the usual hormone markers.

Adult↗
PubMed2002

Biochemical markers of neonatal sepsis: value of procalcitonin in the emergency setting.

BACKGROUND: We evaluated procalcitonin (PCT) assay in the emergency diagnosis of neonatal bacterial infection, especially in preterm infants, relative to C-reactive protein (CRP) and fibrinogen. METHODS: One hundred and twenty neonates (32 preterm), of whom 21 were infected, were tested. RESULTS: Concentrations of PCT, CRP and fibrinogen in uninfected infants were not affected by gestational age at birth. Concentrations of CRP and PCT increased rapidly during the first 24 h of life, while fibrinogen concentrations increased gradually from birth. All marker concentrations were significantly greater in neonates with bacterial infection. Receiver-operating characterstic analysis showed that optimum cut-off values for fibrinogen, CRP and PCT were 3.0 g/L, 7.5 mg/L and 2.5 microg/L respectively, for the diagnosis of sepsis at birth. CONCLUSIONS: Determination of PCT is of value in excluding bacterial infection in neonates since it has a negative predictive value of 93%.

Biomarkers↗
PubMed2002

Placental growth hormones.

Survival and development of the mammalian conceptus depends on a variety of factors. Fetal growth is controlled by genetic and environmental determinants that may limit the mother's capacity to provide an appropriate environment (e.g., space, nutrients, temperature). Exchanges between the mother and fetus take place within the placenta. Interestingly, despite the diversity of mammalian species in terms of placental structure and hormonal functions, placental size at term always correlates with birth weight, reflecting the essential role of this temporary organ. The placenta is the site of major endocrine activity, including synthesis of a broad range of steroid and peptide hormones, growth factors, cytokines, and other bioactive factors. Some of these are produced exclusively by the placenta, including chorionic gonadotropin, and growth hormone (GH)/prolactin-like hormones. This article focuses on the expression, regulation, and physiologic role of placental GHs in mammalian species. Published data suggest that placental GHs are essential for adapting the maternal metabolism to pregnancy, for normal placental development, and therefore for fetal growth.

Animals↗
PubMedDate not supplied

Etiology and outcome of fetal echogenic bowel. Ten years of experience.

OBJECTIVE: To assess the frequency of certain etiologies in fetal echogenic bowel and the related pregnancy outcome. STUDY DESIGN: A retrospective study including 215 cases. Ultrasound findings included bowel abnormality, malformations, growth retardation and Doppler abnormalities. Amniocentesis was performed in 196 cases to screen for abnormalities in karyotype, cystic fibrosis gene and infection. The color of amniotic fluid and a history of first-trimester bleeding were also noted. Outcome according to different etiologies was reported. RESULTS: 112 cases (57%) had a known etiology, which included chromosomal abnormality (7%), infection (4%), cystic fibrosis (1.5%), bowel abnormality (3%), bleeding or stained amniotic fluid (11%), Doppler abnormality (14%), malformation (16%) and miscellaneous (0.5%). Pregnancy was terminated in 39 cases and fetal demise complicated one third of the cases (13) of severe growth retardation. CONCLUSION: Fetal echogenic bowel should be investigated and a careful follow-up is necessary if there is associated Doppler perturbation or growth retardation.

Female↗